Abstract
Role of NFκB in age-related vascular endothelial dysfunction in humans
Highlights
Cardiovascular diseases (CVD) are the leading cause of morbidity and mortality in the United States and other industrialized societies
Recent studies in humans by our group and by others in rodents suggest a critical role of nuclear factor κB (NFκB) in the pro-inflammatory / pro-oxidant linked suppression of endothelial dependent dilation with advancing aging [3,4,5,6,7]
We found that endothelial dependent dilation was impaired in older adults and was associated with increased nuclear translocation of NFκB in their vascular endothelial cells
Summary
Cardiovascular diseases (CVD) are the leading cause of morbidity and mortality in the United States and other industrialized societies. Aging leads to impaired endothelial dependent dilation associated elevated oxidative stress and a proinflammatory endothelial cell phenotype. Recent studies in humans by our group and by others in rodents suggest a critical role of nuclear factor κB (NFκB) in the pro-inflammatory / pro-oxidant linked suppression of endothelial dependent dilation with advancing aging [3,4,5,6,7].
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